| First Author | Boudinot E | Year | 2004 |
| Journal | Respir Physiol Neurobiol | Volume | 140 |
| Issue | 3 | Pages | 231-41 |
| PubMed ID | 15186785 | Mgi Jnum | J:102267 |
| Mgi Id | MGI:3607212 | Doi | 10.1016/j.resp.2004.03.002 |
| Citation | Boudinot E, et al. (2004) Increased ventilation and CO2 chemosensitivity in acetylcholinesterase knockout mice. Respir Physiol Neurobiol 140(3):231-41 |
| abstractText | To investigate the effects of a permanent excess of acetylcholine (AChE) on respiration, breathing and chemosensitivity were analyzed from birth to adulthood in mice lacking the AChE gene (AChE-/-), in heterozygotes, and in control wild-type (AChE+/+) littermates. Breathing at rest and ventilatory responses to brief exposures to hypoxia (10% O2) and hypercapnia (3-5% CO2) were measured by whole-body plethysmography. At rest AChE-/- mice show larger tidal volumes (VT, + 96% in adults), overall ventilation (VE, + 70%), and mean inspiratory flow (+270%) than wild-type mice, with no change in breathing frequency (fR). AChE-/- mice have a slightly blunted response to hypoxia, but increased VE and fR responses to hypercapnia. Heterozygous animals present no consistent alterations of breathing at rest and chemosensitivity is normal. Adult AChE-/- mice have an increased VE/VO2 and a marginally higher normalized VO2. The results suggest that the hyperventilation and altered chemosensitivity in AChE-/- mice largely reflect alterations of central respiratory control. |
